The overproduction and accumulation of amyloid-β (Aβ) peptide and hyperphosphorylated tau (p-tau) protein are the two most common hypotheses for AD pathogenesis, but recent findings have demonstrated that chronic oxidative stress, hormone imbalance, mitochondrial dysfunction, inflammation, calcium mishandling, mitotic dysfunction, genetic components or blood–brain barrier (BBB) dysfunction also likely play key roles in the disease process [7, 8]. Here, MAPT is linked to Alzheimer disease.